P-162: Pathophysiology of Endometriosis is Interacted by MIF, its Receptor and COX-2
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Abstract:
Background: Endometriosis is a gynecological disease associated with severe pelvic pain and infertility. Immunological changes that occur in patients with endometriosis include reduced natural killer cell and T-lymphocyte cytotoxicity in the peritoneal fluid, and an elevated number of activated macrophages. MIF via its receptor, CD74, initiates a signaling cascade that leads to proliferation and survival of cells. Also, MIF binding to CD74 activates p38 signaling pathways that leads to positive effect on the expression of COX-2. In this study, the expression of MIF, CD74 and COX-2 genes in eutopic, ectopic and the normal endometrium was evaluated in menstrual cycle by Q-PCR. The expression level of MIF protein in peripheral blood samples of patients was another variable factor checked in this study. Materials and Methods: All women taking part in this study, were between 20-45 years old, had no endometrial hyperplasia or neoplasia. Twelve ectopic and 8 eutopic endometriosis samples and 12 normal endometrium during menstrual cycle as control group were tested in this study. Peripheral blood samples were likely obtained from each group. The level of MIF, CD74 and COX-2 genes expression was investigated. Also, protein level of MIF in blood serum were measured by ELISA assay. Results: The expression of MIF, CD74 and COX-2 genes in ectopic, eutopic and normal endometrium during menstrual cycle were varied. Also women with endometriosis had higher circulating levels of MIF protein as compared to normal controls. Conclusion: Higher expression of MIF, CD74 and COX- 2 genes in ectopic endometrium can be considered as a molecular biomarker for endometriosis development and pathophysiology. Variation in the expression of these genes in normal endometrium during menstrual cycle could play an essential role in reproduction, inflammation and endometrium reconstruction. Also, high level of MIF in blood serum in endometriosis could act as a biomarker in diagnosis of endometriosis.
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Journal title
volume 7 issue 3
pages 98- 98
publication date 2013-09-01
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